Recent studies from this laboratory on chronic alcoholics with rhabdomyolysis suggest a possible etiologic role of phosphorus deficiency. Additional studies on dogs have shown that modest phosphorus deficiency (15%) induces abnormal elevation of water, sodium and chloride in the muscle cell and a decline of its resting membrane potential. Unlike alcoholic patients whose muscle P was 50% of normal, the dogs were only modestly P-deficient and did not display overt rhabdomyolysis. This research is proposed to provide information on the following questions: 1) Does the alcoholic dog develop a myopathy? 2) Does the alcoholic dog become phosphorus deficient? 3) If P-deficiency occurs in the alcoholic dog, what is the mechanism of lowering P concentration? 4) Does P-deficiency in the dog cause overt rhabdomyolysis? 5) Does the myopathy in the P-deficient dog occur independently of other derangements in the muscle cell? 6) Does alteration of biophysical properties of the cell (ion permeability; resting membrane potential) precede alterations of ionic composition? 7) What is the effect of alcoholism or independently, phosphorus deficiency on non-ionic components (myoglobin, ATP, CP and creatinine) of the muscle cell? 8) What is the role of malnutrition in the myopathy of alcoholism or phosphorus deficiency? 9) What is the role of starvation or refeeding in the myopathy of alcoholism or P-deficiency? 10) Does P-supplementation in the dog prevent alcoholic myopathy? 11) If other ions (e.g., Mg, K) become deficient in alcoholic or P-deficient dogs, will appropriate supplementation of these ions prevent myopathy? 12) does acute hypophosphatemia and respiratory alkalosis in the alcoholic dog correlate with the appearance of acute rhabdomyolysis? 13) Does muscle become hypermetabolic with chronic alcoholism like that putatively occurring in the liver, red cell and brain? 14) Muscular work possibly enhances the likelihood of alcoholic cardiomyopathy. Does the same relationship pertain to myopathy? Is exercise hyperemia impaired, thus inducing ischemic injury?